The role of Th17 and Treg cells in normal pregnancy and unexplained recurrent spontaneous abortion (URSA): New insights into immune mechanisms
- PMID: 37603948
- DOI: 10.1016/j.placenta.2023.08.065
The role of Th17 and Treg cells in normal pregnancy and unexplained recurrent spontaneous abortion (URSA): New insights into immune mechanisms
Abstract
Recurrent spontaneous abortion (RSA) has various causes, including chromosomal abnormalities, a prethrombotic state, and abnormal uterine anatomical factors. However, in about 50% of cases, the cause remains unknown and is referred to as unexplained recurrent spontaneous abortion (URSA). The fetus is protected from rejection by the maternal system, acting as an allogeneic gene, and immune tolerance serves as a crucial mechanism. The Th17/Treg cell paradigm's emergence as a new subpopulation of CD4+ T cells, interacting with one another, plays an essential role in the immune microenvironment and the body's defense system. This Th17/Treg cell model helps to explain the pathology of recurrent miscarriage that could not be accounted for by the original immune mechanism based on the Th1/Th2 model. Furthermore, the plasticity of Th17 and Treg cells holds innovative significance in autoimmunity and abortion. This paper reviews the role of Th17/Treg cellular immune response in the maintaining normal pregnancy and understanding unexplained recurrent spontaneous abortion.
Keywords: Immune reaction; Maternal-fetal tolerance; Th17 cells; Treg cells; Unexplained recurrent spontaneous abortion.
Copyright © 2023 The Authors. Published by Elsevier Ltd.. All rights reserved.
Conflict of interest statement
6 Declaration of competing interest Declarations of interest: none! The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential. conflict of interest. 7 Author Contributions Cen Tang conducted research and wrote the article, and Wanqin Hu provided direction and ideas. All authors have read and approved the final manuscript. Cen Tang is the First Author and Wanqin Hu is the Correspondent Author. 8Funding This work has been supported by the National Natural Science Foundation of China. (No. 82060294) 9Acknowledgments We are grateful to the participants for their contribution in accomplishing this study.
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